50 HIRST 



necessary break in the cell membrane to permit virus entry. The evi- 

 dence for this is very meager. It is known that the removal of receptors 

 bares other, possibly deeper structures of the cell (Burnet and Ander- 

 son, 1947). It has been found that immediately after adsorption of 

 virus to susceptible cells, the agent can be eluted by treating with bac- 

 terial enzyme preparations but that within a short time the virus dis- 

 appears and is no longer elutable. The infectious process is accompanied 

 by receptor (inhibitor) destruction (Schlesinger, 1950). All active 

 strains of the MNI group possess the receptor destroying property. 

 None of these facts eliminate the possibility that receptor destruction 

 is an unnecessary side reaction of the infectious process. The strongest 

 argument for the utility of this reaction for the virus economy is the 

 unlikelihood of finding a vestigial process so prominent and uniformly 

 present in an organism which is otherwise stripped below the essentials 

 necessary for independent existence. 



St. Groth has raised the only objections thus far to the foregoing 

 hypothesis, but most of his conclusions seem too poorly documented to 

 warrant a detailed discussion. His main argument is that periodate 

 treated cells of the chorioallantoic membrane have receptors which can- 

 not be destroyed by virus (Fazekas de St. Groth and Graham, 1949), 

 yet the cells are readily infectible. This has not been substantiated by 

 Schlesinger who found that under the prescribed conditions the recep- 

 tors were, in fact, destroyed by virus (unpublished observations). The 

 second approach (Fazekas de St. Groth, 1948) was more interesting 

 than the first, though it would be helpful if the observations were con- 

 firmed and extended. He infected the cells of the chorioallantoic mem- 

 brane and found that immediately after adsorption most of the adsorbed 

 virus could be eluted through the use of bacterial filtrate. Within 

 an hour or two the elutable virus had decreased to zero. Indicator 

 virus, which cannot destroy receptors, "disappeared" (became non- 

 elutable) at the same rate. This experiment, of course, does not deny 

 the necessity of enzymatic action on receptors for the virus to enter 

 the cell. The possibility should also be considered that the enzyme may 

 function within the cell although it is not certain that inhibitor is 

 found there. 



LITERATURE CITED 



Anderson, S. G., 1948. Mucins and Mucoids in Relation to Influenza Virus Action 

 1. Inactivation by RDE and by Viruses of the Influenza Group of Serum Inhibi- 

 tor of Hemagglutination. Austral. J. Exptl. Biol, and Med. Sci., 26, 347-354- 



Burnet, F. M., 1945. Hemagglutination by Mumps Virus: Relationship to Newcastle 

 Disease and Influenza Viruses. Austral. J. Sci., 8, 81-83. 



Burnet, F. M. and Anderson, S. G., 1947. The "T" Antigen of Guinea Pig and Human 

 Red Cells. Austral. J. Exptl. Biol, and Med. Sci., 25, 213-217. 



